The progression of synovial inflammation and joint destruction in rheumatoid arthritis (RA) is characterized by a pronounced tumor-like expansion of the synovium. Neovascularization, which may play a pivotal role in the physiological and pathological condition, is a complex process involving endothelial cell division, selective degradation of vascular basement membranes and the surrounding extracellular matrix, and endothelial cell migration. The involvement of several endogenous molecules has been purported based on the ability of these molecules to regulate the proliferation of endothelial cells. Moreover, a number of factors which regulate both angiogenic and angiostatic functions may be crucial in promoting neovascularisation. These include vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), angiopoietins and chemokine family such as CXCL8 and CXCL10. This review will discuss the expression and regulation of these angiogenic and angiostatic cytokines in the context of chronic inflammatory arthritis such as RA and experimental arthritis.
Keywords: Cytokines, Rheumatoid Arthritis, Therapeutic Targets, synovial inflammation, tumor, Neovascularization, endothelial cell, proliferation, Angiogenesis, Synovial membrane
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